Systemic inflammation is greater in individuals with concurrent TB and diabetes than in euglycemic individuals with TB, and this disparity persists through the full 6-month course of anti-tubercular treatment.
Skin inflammation in Sharpin-deficient mice is primarily due to TNFR1-dependent apoptosis, but necroptosis appears to play a bigger role in inflammation of internal organs.
A link between chronic stress and organ dysfunction is explained by the gateway reflex, in which brain micro-inflammation at specific vessels establishes a new neural pathway to induce fatal organ failure particularly in gastrointestine and heart.
Reduced energy expenditure in obesity may result from reduced sensitivity to sympathetic activation due to inflammation-generated signals in adipose tissue.
During aging, the pancreatic endocrine islets undergo chronic inflammation, which is associated with a reduced capacity for self-renewal of the insulin-producing beta-cells in zebrafish.
The adaptor proteins FADD and TRADD play an important role in the Sharpin-dependent anti-apoptosis signaling pathway in keratinocytes and regulate skin homeostasis.
A single neonatal inflammatory event induces long-term impairments in two forms of adult respiratory motor plasticity, an important aspect of the control of breathing for compensation after injury or disease.
